Adverse drug reactions (ADRs) are usefully separated into type A reactions (predictable from known pharmacologic properties and largely dose related) and type B reactions (unpredictable and restricted to a vulnerable subpopulation). Type B reactions comprise 10% to 15% of all ADRs and include immunologic drug reactions, drug intolerance (eg, tinnitus after single aspirin tablet), and idiosyncratic reactions, some of which are pseudoallergic (eg, aspirininduced reactions). Immune mechanisms are thought to be involved in 6% to 10% of all ADRs. Allergenic drugs can induce the entire spectrum of immunopathologic reactions, which are clinically indistinguishable from reactions elicited by foreign macromolecules (Table 206.1). Gell and Coombs' type I reactions are caused by drug/antigen-specific immunoglobulin E (IgE) that binds to high-affinity Fc-IgE receptors on mast cells and basophils. Cross-linking these receptors leads to the release of vasoactive mediators such as histamine and cysteinyl leukotrienes. Typical syndromes include urticaria, anaphylaxis, rhinitis, and bronchoconstriction, which can occur immediately in a previously sensitized individual. Type II cytolytic reactions are generally confined to rapidly haptenating drugs such as penicillins and are based on immunoglobulin G (IgG)-mediated cytotoxic mechanisms, resulting mainly in blood cell cytopenias. Type III reactions are immune complex mediated and may involve complement activation and stimulation of Fc-α receptor– activated inflammatory cells. Drug-specific immune complexes result from high-dose, prolonged therapy and may produce drug fever, a classic serum sickness syndrome, and various forms of cutaneous vasculitis.
|Original language||English (US)|
|Title of host publication||Clinical Infectious Disease|
|Publisher||Cambridge University Press|
|Number of pages||12|
|State||Published - Jan 1 2010|
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